Liability For Prenatal Harm in The Workplace - The Need For Reform

Liability for Prenatal Harm in the Workplace:
The Need for Reform*
Steven S. Paskal**
I. INTRODUCTION
Fifteen percent of all recognized pregnancies result in spon-

taneous abortion' and seven percent of liveborn infants are
afflicted with birth defects.2 Although there are innumerable
workplace stressors that are known or suspected to cause such
injuries, there have been very few prenatal injury lawsuits
brought against employers to date.3 In the last fifteen years,
however, considerable attention has been focused on the issue,4
and the frequency of such lawsuits can be expected to increase.
This Article describes the causes of action available under
current Washington law when a workplace hazard contributes
to an adverse reproductive outcome such as miscarriage, birth
defects, transplacental carcinogenesis, or other prenatal
injury.5 Part II delineates the wide variety of workplace condi-
tions that may lead to an adverse reproductive outcome, rang-
* © Steven S. Paskal, 1994

** B.S. Chemistry 1978, Old Dominion University; M.S. Industrial Environmental
Health 1979, University of Pittsburgh; Certified in Comprehensive Practice of
Industrial Hygiene 1984, American Board of Industrial Hygiene; J.D. 1988, Georgetown
University Law Center. Mr. Paskal practices employment law in Olympia, Washington.
He also practices as an Environmental Health Consultant.
1. OFFICE OF TECHNOLOGY ASSESSMENT, REPRODUCTIVE HEALTH HAZARDS IN THE
WORKPLACE 343 (1985) [hereinafter OTA].
2. Id. at 60.
3. As of this writing, approximately one dozen prenatal injury cases had been
reported.
4. See, e.g., Emily Buss, Getting Beyond Discrimination:A Regulatory Solution to
the Problem of Fetal Hazardsin the Workplace, 95 YALE L.J. 577 (1986); Lynne Darcy,
Birth Defects Caused by ParentalExposure to Workplace Hazards:The Interface of Title
VII with OSHA and Tort Law, 12 J.L. REFORM 237 (1979); Valerie Mark, The Flip Side
of Fetal ProtectionPolicies:CompensatingChildren Injured Through ParentalExposure
to Reproductive Hazards in the Workplace, 22 GOLDEN GATE U. L. REV. 673 (1992);
Steven S. Paskal, Dilemma:Save the Fetus or Sue the Employer, 39 LAB. L.J. 323 (1988);
Wendy W. Williams, Firingthe Woman to Protect the Fetus: The Reconciliationof Fetal
Protection with Employment Opportunity Goals Under Title VII, 69 GEO. L.J. 641
(1981).
5. It does not address the related issue of employee reproductive health (sterility,
loss of libido).
283
284 University of Puget Sound Law Review [Vol. 17:283
ing from emotional stress, cigarette smoke, and fall hazards to

more traditional teratogen exposures such as lead. Part III
describes the types of reproductive harm that can form the
basis of a lawsuit in Washington. Part IV notes the theories of
liability and the potential defendants, including employers, co-
employees, consultants, manufacturers, and others contributing
to such an outcome. Part IV also offers a prediction that the
number of lawsuits alleging such injury are likely to increase
dramatically. Part V discusses defenses available to an
employer. Part VI identifies the goals that should be served
under any proposed solution. Finally, Part VII argues for a leg-
islative approach towards an equitable balancing of childrens'
health interests against womens' employment opportunities
and employers' concerns about massive tort liability.
II. PRENATAL HARM IN THE WORKPLACE
Most people's conception of prenatal injury revolves around

images of children born with missing or shortened limbs
because of their mothers' exposure to teratogenic chemicals.
These extreme examples, however, are but a small part of a
wide spectrum of prenatal injuries attributable to an even wider
assortment of occupational conditions. For an attorney or legis-
lator to comprehend the true magnitude of the potential liabil-
ity faced by today's employer one must look at the larger
picture. This is best accomplished by tracking human reproduc-
tion and pointing out the stages where an occupational insult
can cause disruption and injury. For the sake of simplicity, this
Article will discuss only fertilization and development leading
to a single child.6
A. Preconception CongenitalInjury
Conception begins when one gamete from each parent join.'
The male contributes spermatozoa containing half of the genetic
material that will direct the development of the child.' Sperma-
tozoa originate from a normally inexhaustible pool of progenitor
cells in the testes. 9 These progenitor cells number in the many
millions and routinely divide and subdivide to produce new
6. See generally STANLEY W. JACOB ET AL., STRucTuRE AND FUNCTION IN MAN

(1978). This reference forms the basis for the following discussion of the biology of
reproduction.
7. Id. at 584.
8. Id. at 582, 584.
9. Id. at 580-81.
1994] PrenatalHarm in the Workplace 285
spermatozoa for fertilization.1" The average ejaculation con-

tains 200 to 300 million spermatozoa of which only one will fer-
tilize the female's ovum.'1 Throughout his life, the male's
sperm cells, at various stages of maturation, are vulnerable to
chemical or physical disturbances that may alter their genetic
material in such a way that fertilization will not be successful
12
or will lead to a defect in the child.
Many chemicals as well as ionizing radiation have been
shown to4 cause aberrations in spermatozoa.' 3 While no
"marker" genetic disorders have been isolated for specific
exposures, epidemiological studies have correlated several occu-
5
pations with above average incidences of certain birth defects'
as well as with higher rates of miscarriage among the spouses of
exposed males.' 6 Paternally-mediated prenatal harm has also
been alleged in civil suits.' 7
10. Id. at 580.

11. Id. at 581.
12. OTA, supra note 1, at 47.
13. See id. at 69-125. A review of the literature showed that abnormal spermatozoa
may be caused by several exposures, including arsenic, chloroprene, lead, kepone, and
ionizing radiation. Id.
14. A "marker" disorder is one that is definitively attributable to a specific
exposure.
15. See Andrew F. Olshan et al., PaternalOccupation and CongenitalAnomalies in
Offspring, 20 Am. J. INDUS. MED. 447 (1991). Dr. Olshan's epidemiological study
correlates increased incidence of specific congenital anomalies with paternal
occupations. Noted associations include the following: (1) janitor with hydrocephaly
and heart defects; (2) forestry and logging workers with cataracts, heart valve problems,
and fused fingers; (3) printers with clubfoot and urethral defects; and (4) plywood
workers with dislocated hips, heart defects, and stomach defects. Id.; see also David A.
Savitz & Jianhua Chen, Parental Occupation and Childhood Cancer & Review of
Epidemiologic Studies, 88 ENVTL. HLTH. PERSP. 325 (1990) (reviewing epidemiological
literature and noting that "[s]everal associations have been found with consistency:
paternal exposures in hydrocarbon-associated occupations, the petroleum and chemical
industries and especially paint exposures have been associated with brain cancer; paint
exposures have also been linked to leukemias").
16. T.N. Tanenbaum & R.J. Goldberg, Exposure to Anesthetic Gases and
Reproductive Outcome, 27 J. OccuP. MED. 659 (1985) (noting an increase in spousal
miscarriage rate associated with paternal exposure to waste anesthetic agents).
17. Monaco v. United States, 661 F.2d 129 (9th Cir. 1981) (alleging that daughter
of a U.S. serviceman was born with a birth defect known as arterio-venous anomaly in
the brain attributable to the father's exposure to radiation from a research laboratory
working on the "Manhattan Project" during World War II); In re Agent Orange Prod.
Liab. Litig., 506 F. Supp. 762 (E.D.N.Y. 1980) (alleging that Vietnam veterans'
exposures to herbicides caused genetic malformations resulting in children's birth
defects); Stelly v. Firestone Tire & Rubber Co., 20 O.S.H. Rep. (BNA) 1040 (Tex. Dist.
Ct. Oct. 21, 1990) (alleging father's exposure to mercury caused child's mental
retardation).
The female contributes one of a finite number of ova, each

of which, like the spermatozoon, contains half of the genetic
material of the new child.'" The female's supply of ova is fixed
from conception and declines with age. 9 By the age of sixteen
or so, when a woman can be expected to enter the work force,
the number of oogonia (Greek for parents of eggs) number less
than 400.20 These "parent" cells are frozen in a stage of cell
division. 2 1 Every ovarian cycle (approximately twenty-eight
days) about twenty oogonia proceed through the last stages of 22
division, but only one reaches the mature stage of an ovum.
The same types of chromosomal damage that affect the sperma-
tozoa can similarly impact the ova before they are fertilized and
with similar consequences. 2 3
B. Miscarriage
At ovulation, the surviving, dominant ovum is released
from its housing, the follicle, and proceeds through the oviduct,
where it may be fertilized by the entry of one spermatozoon.2 4
Once the ovum is fertilized, it becomes a "zygote" and proceeds
to divide and grow. 25 Given proper genetic guidance, adequate
nutrients, and correct hormonal stimuli from the mother's endo-
crine system, the zygote will implant in the endometrial lining
of the uterus and begin to grow. 26 While custom varies some-
what, the general rule is that the developing child is termed a
zygote through the third week of pregnancy, an embryo during
weeks three through eight, and a fetus thereafter until birth.
The point at which the fetus becomes viable is generally 28
pre-
sumed to be at twenty weeks and 500 grams (1.1 lbs.).
18. OTA, supra note 1, at 48-49.

19. R. BERKOW & A. FLETCHER, THE MERCK MANUAL OF DIAGNOSIS AND THERAPY
1683 (1987).
21. Id.
22. Id.
23. See, e.g., id. at 67-126 (comparing the toxic effects on sperm and ova).
24. Id. at 49-50.
25. Id.
26. Id.
27. Id. at 49.
28. JACOB et al., supra note 6, at 592. The point of transition to viability (when the
fetus can survive outside the mother) is significant because it may determine whether
the fetus has achieved person status under the law. Different jurisdictions that have
ruled on this issue have reached different results. Some have adopted a bright-line
demarcation as a matter of law of the 1st trimester (approximately 28 weeks). Roe v.
Wade, 410 U.S. 113, 162-65 (1973). Others have considered the issue a fact question for
trial. Georgia hinges the personhood question on the date the conceptus is "quick" (first
If the genetic material of the spermatozoon or the ovum has

been interfered with by chemicals or radiation in a manner that
has significantly diminished its integrity, the conceptus will not
successfully implant and flourish in the endometrium of the
mother.2 9 In human populations, the types and severity of
parental exposures (or other factors) that can prevent the suc-
cessful implantation of fertilized ova is open to speculation.
This is because embryos that do not implant and survive for a
week or so are neither detected nor counted in epidemiologic
studies as a miscarriage. °
While genetic harm that prevents successful implantation
may be hard to measure, such harm can also lead to later mis-
carriages that are more easily documented and epidemiologi-
cally correlated with many workplace factors.3 1 Even
exposures as widespread as to video display terminals are sus-
pected of causing increased miscarriage rates.3 2 Of note is the
felt to move by the mother, generally around the 16th week), but the determination is
submitted as a question of fact to the jury. Porter v. Lassiter, 87 S.E.2d 100, 103 (Ga.
Ct. App. 1955). The medical literature is becoming murkier because technology is
increasingly able to supplant maternal support mechanisms for preterm babies. To
complicate matters further, not all researchers use the same cutoff in epidemiological
studies of miscarriage.
29. This phenomenon forms the basis for the "dominant-lethal" test of
mutagenicity in which male mice or rats are given an injection of the substance of
concern and then mated with a series of unexposed females. The females are then
sacrificed and the number of dead or resorbing fetuses are determined. Elevations in
these early "miscarriage" rates are taken as evidence of mutagenicity (damage to the
chromosomes of the sperm). The predominant effect of sperm mutation is the death of
the embryo. LoDuis CA SAi-r & JonN DouLL, TOXicOLOcY: TuR Bpaic Seieiv oF
POISONS 315 (1975).
30. OTA, supra note 1, at 51. It is estimated that approximately 50% of fertilized
ova are lost in the first one to two weeks of development. Epidemiologic studies of
miscarriage focus on recognizable pregnancies (those lasting more than two to three
weeks).
31. Epidemiological studies correlating elevated miscarriage (1st trimester) rates
with maternal occupations and exposures abound, even for traditionally clean
industries such as electronics. See, e.g., Jane A. Lipscomb et al., Pregnancy Outcomes
in Women Potentially Exposed to Occupational Solvents and Women Working in the
Electronics Industry, 33 J. OccuP. MED. 597 (reporting a greater than four-fold risk in
spontaneous abortion among women reporting regular solvent exposure over population
average); Gayle C. Windham et al., Exposure to Occupational Solvents and Adverse
Pregnancy Outcome, 20 AM. J. INDPUS. MED. 241 (1991) (identifying miscarriage rates
4.7, 3.1, and 2.3 times the background (control population) among women working with
perchloroethylene, trichloroethylene, and paint thinners, respectively); Jun Zhang et
al., OccupationalHazards and Pregnancy Outcomes, 21 AM. J. INDUS. MED. 397 (1992)
(correlating maternal occupational exposure to noise, radiation, and chemicals with
increases in the rates of antepartum death).
32. See Study Links Increased Miscarriage Risk to Workers with High Magnetic
Field Exposure, 22 O.S.H. Rep. (BNA) 1314 (1992) (noting a study of three companies in
histologic finding that a large percentage of spontaneous abor-

tions show chromosomal abnormalities that are incompatible
with life. 3 Accordingly, lawsuits alleging miscarriage and
early death because of maternal exposures are beginning to
make their way through the courts.3 4
C. Disruption of Organogenesis
During the first twelve weeks, the embryo undergoes orga-
nogenesis, literally the birth of its organs. 35 This process is a
very precise, genetically programmed sequence of accelerated
cell division and differentiation that results in the conversion of
a single amorphous cell mass into a rudimentary anthropomor-
phic organism with all the proper parts.36 The only organ sys-
tems that are not completely formed by the twelfth week are
the central nervous system and genitalia, which continue to
grow and develop until even after birth. If this process is
interfered with, the result can be undesirable gross congenital
malformations that have been labeled terata (literally,
38
monsters).
During organogenesis, timing is everything. Chemical or
physical teratogens (radiation, therapeutic drugs, industrial
pollutants) may have completely different effects depending on
Finland that revealed that the use of VDTs having high magnetic fields during early
pregnancy correlated with an increased rate of miscarriage). But see Teresa M. Schnorr
et al., Video Display Terminals and the Risk of Spontaneous Abortion, 324 NEW ENG. J.
MED. 727 (1991) (finding no excess risk of spontaneous abortion among women who
used VDTs during the 1st trimester of pregnancy).
33. See BERKOW & FLETCHER, supra note 19, at 1759. "Since in 60% of spontaneous
abortions the fetus is either absent or grossly malformed, and in 25 to 60% it can be
found to have chromosomal abnormalities incompatible with life, spontaneous abortion
may be a natural rejection of a maldeveloping fetus." Id. A finding of such
chromosomal damage in the aborted fetus of an employee in conjunction with the
presence of a mutagenic stressor in the workplace, may serve as the evidence of
causation in a lawsuit for wrongful death (assuming the jurisdiction recognizes such
actions for miscarriages).
34. Dwyer v. West Bradford Corp., 591 N.Y.S.2d 92 (App. Div. 1992) (alleging office
worker's miscarriage was caused by carbon monoxide leakage from boiler system into
office); see also Rodriguez v. Mallory Capacitor Co., 21 O.S.H. Rep. (BNA) 498 (Tex. Dist.
Ct. Sept. 23, 1991) (alleging that workplace exposure of the mothers to unspecified
chemicals caused miscarriages and birth defects ranging from mental retardation to
physical deformities).
35. JACOB et al., supra note 6, at 588.
36. Id. at 588-90.
38. TABER's CYCLOPEDIC MEDICAL DICTIONARY 1835 (16th ed. 1989) [hereinafter
TABER's]
the day incurred. 39 Dramatic manifestations of this phenome-

non can be elicited in animal studies.40 For example, when
pregnant rats are given excessive doses of vitamin A on day
eight of gestation, skeletal malformations result, while if given
on day twelve, the same dose results in cleft palate formation. 4 '
Technically, teratogenesis is limited to this stage of
development. 42
The most dramatic human experience with teratogens has
been associated with pharmaceuticals, of which thalidomide is
the most notorious. Thalidomide is a mild sedative that was
harmless to pregnant women except between days thirty-five
and fifty of pregnancy.43 Unfortunately, approximately 10,000
European women, unaware of the risks, took thalidomide dur-
ing that thirty-five to fifty day period and gave birth to children
with phocomelia.44 Pharmaceuticals have also been the most
litigated of human teratogens, including Thalidomide,4 5
Bendectin,"6 Dilantin, 47 and spermicidal jellies."
Several nonpharmaceuticals have also been implicated as
teratogens based on animal studies or epidemiological data.49
Interestingly, the only litigation involving workplace exposure
to a teratogen involved one of the best known, rubella, and was
39. CAsARErr & DOULL, supra note 29, at 318.

40. Id. at 319.
41. Id. at 318-19.
42. Id. at 314. In Greek, teratogenesis means literally the "birth of monsters."
TABER'S, supra note 38, at 1835-36.
43. CASARETT & DOULL, supra note 29, at 313.
44. Id. Phocomelia describes a congenital malformation wherein the long bones in
the extremities are absent or poorly developed. TABER'S, supra note 38, at 1388.
45. Henry v. Richardson-Merrell, Inc., 366 F. Supp. 1192 (D.N.J. 1973).
46. Oxendine v. Merrell Dow Pharmaceuticals, Inc., 506 A.2d 1100 (D.C. 1986).
47. Harbeson v. Park Davis, Inc., 98 Wash. 2d 460, 656 P.2d 483 (1983).
48. Wells v. Ortho Pharmaceutical Corp., 615 F. Supp. 262 (N.D. Ga. 1985).
49. Known teratogens that may be encountered in the workplace include
antineoplastic agents to which health care workers may be exposed. BERKOW &
FLETCHER, supra note 19, at 1752. Such drugs have the intended effect of disrupting the
rapid growth of tumors; an outcome that is disastrous during the period of fetal
organogenesis. Id. at 1911. Rubella (German measles) is also a well-known teratogen
that can easily infect the fetus during organogenesis resulting in a wide range of
congenital anomalies. See id. at 1752. Animal studies have shown a great number of
materials to be potential teratogens: acrylonitrile, arsenic, benzene, benzo-a-pyrene,
boron anhydride, cadmium dusts and salts, carbon disulfide, chloroform, chloroprene,
chromium, copper dusts and mists, cyanides, di-n-butylphthalate, ethylene glycol mono-
ethyl/methyl ethers, formamides, fungicides/fumigants/sterilants (most), inorganic
mercury, methyl chloride, nickel, organic mercury, pesticides (most), selenium, vinyl
chloride, and xylenes. M. PAUL, OCCUPATIONAL AND ENVIRONMENTAL REPRODUCTIVE
HAzARDs: A GUIDE FOR CLINICIANS 394-406 (1992).
the first such case reported in the United States.5" As more

attention is focused on the teratogenic potential of workplace
exposures, it can be expected that litigation involving
nonpharmaceutical-based teratogenesis will increase.
Chemical or biological agents are not the only way to affect
teratogenesis. In fact, one of the most common and potent ter-
atogens is ordinary heat. 5 1 Additionally, ionizing radiation dis-
rupts rapid cellular growth and can disrupt organogenesis.5 2
D. Fetal Injury
The growing fetus is encased in a placenta upon which it
relies for nutrients and elimination of metabolic waste prod-
ucts. 5 3 This structure also serves to cushion and protect the
fetus. 5 4 Maternal and fetal blood do not merge in the pla-
centa.55 Rather, fetal capillaries protrude into pools of mater-
nal blood, allowing the diffusion of gases and smaller
particulates from the mother's blood into the fetus's blood.5 6
This system can screen large molecules or bacteria but not
smaller substances such as viruses or most workplace chemicals
57
or metals.
For approximately thirty weeks following organogenesis,
the fetus will remain dependent on the placenta.5 8 If the pla-
centa is damaged or insufficient nutrients are directed through
it, the fetus will be deprived of the necessary life support.5 9
During this stage, fetotoxicity may occur whereby the mother's
50. Dillon v. S. S. Kresge Co., 192 N.W.2d 661 (Mich. Ct. App. 1971) (alleging that
employer's failure to maintain sanitary conditions caused pregnant employee to
contract rubella and resulted in birth defects in child).
51. Jacqueline Agnew et al., Reproductive Hazards of Fire Fighting I: Non-
chemical Hazards, 19 AM. J. INDUS. MED. 433, 434-37 (1991) (collecting toxicological and
epidemiological literature). A rise in core temperature above 38.9"C is thought to pose a
teratogenic hazard. Id. at 436-37. It has been reported that one of the greatest fears of
toxicologists involved in teratology is that the thermal regulation of some test animals'
cages will malfunction. CASARETT & DouLL, supra note 29, at 328.
52. See Agnew et al., supra note 51, at 440.
53. JACOB et al., supra note 6, at 591.
54. Id.
55. Id.
56. Id.
57. MARK EvANs, REPRODUCTIVE RIsKS AND PRENATAL DIAGNosIs 47-48 (1992). In
fact, some chemicals, such as carbon monoxide, may attain higher concentrations in the
fetal blood than in that of the mother. Melissa A. McDiarmid et al., Reproductive
Hazards of FireFightingI. Chemical Hazards, 19 AM. J. INDUS. MED. 458, 447 (1991).
59. JACOBS et al., supra note 6, at 591.
workplace exposure to toxins is transmitted to the fetus result-

ing in injury. 0
The effect on a fetus of a transplacental toxic exposure will
depend on the type of exposure. 6 ' For carcinogens and many
chronically toxic substances that increase lifetime risk of illness
in some proportion to the long-term dosage, the relatively brief
in utero exposure may not be as significant as that of the
mother during her working career. 62 On the th other hand, the
mother may have lower susceptibility due to more developed
defense and repair mechanisms.6 3
There is an extensive base of scientific literature respecting
transplacental migration and toxicity of various chemical com-
pounds, including animal and human studies. 4 There has been
litigation alleging direct, post-organogenesis injury to the fetus
caused by workplace exposures of the mother to several agents,
including carbon monoxide,6 5 mercury,6 6 and hepatitis6 7 as well
as "unspecified contaminants.""8
More complex scenarios exist in which conduct towards the
mother can result in toxic injury to a fetus. An example is the

61. EvANs, supra note 57, at 47-48; OTA, supra note 1, at 56-57.
62. EvANs, supra note 57, at 91-94.
63. One notable defense mechanism is the blood-brain barrier which, in the adult,
limits the infiltration of certain substances. In the child, this barrier is less developed.
One effect of this difference is observed with inorganic lead. In adults, because of the
blood-brain barrier, lead is distributed from the blood to the peripheral nervous system
causing peripheral neuropathy ("wrist drop"). In children, however, the lead
accumulates in the brain causing mental defects. CmsARz"r & DouLL, supra note 29, at
36, 151. Epidemiological studies have suggested increased risks of childhood cancer
among the offspring of parents in several occupations (mechanics, aircraft workers,
military personnel, painters, chemical workers, welders, pharmacists, physicians, and
machinists). Savitz & Chen, supra note 15, at 325.
64. See McDiarmid et al., supra note 57, at 454-56.
65. Thompson v. Pizza Hut of America, 767 F. Supp. 916 (N.D. Ill. 1991) (alleging
that mother's exposure to carbon monoxide and other fumes resulted in child's birth
defects).
66. Namislo v. Akzo Chem., Inc., 620 So. 2d 573 (Ala. 1993) (alleging that
employer's negligent exposure of pregnant mother to mercury caused child's mercury
poisoning).
67. Jarvis v. Providence Hosp., 444 N.W.2d 236 (Mich. Ct. App. 1989) (alleging in
wrongful death action that stillborn birth was due to mother's exposure to hepatitis
during 23rd week of pregnancy where the mother, a laboratory technician, was
diagnosed as having contracted hepatitis during 8th month and delivered a stillborn
baby).
68. See Rodriguez v. Mallory Capacitor Co., 21 O.S.H. Rep. (BNA) 498 (Tex. Dist.
Ct. Sept. 23, 1991) (alleging that employer's negligence caused, inter alia,birth defects
including mental retardation and physical deformities among the children of
approximately 50 employees).
case where a woman whose blood does not contain a protein

called the Rh factor is given a transfusion of blood that does
contain this component, causing her body to produce Rh antibo-
dies.6 9 If she subsequently conceives a child who does carry this
genetically dictated factor, her placenta will infuse the fetus
with an allergy to its own blood.70
Of course, simple physical forces can injure the fetus as
well. There have been lawsuits where trauma to the employee/
mother has resulted in fetal injury7 ' or death. 72 Less dramatic
are the plethora of exposures associated with the birth of a baby
that is premature or small for its gestational age. 73 In the lat-
ter case, while no direct injury may be said to have occurred,
the baby is more vulnerable to a variety of problems.74
E. Postpartum Injury
Even after birth, the child can still suffer injury due to the
mother's exposure. For example, newborns that are breast-fed
69. BERKOW & FLETCHER, supra note 19, at 1132.

70. Renslow v. Mennonite Hosp., 351 N.E.2d 870 (Ill. App. Ct. 1976). Renslow is a
landmark case in which preconception liability to the injured fetus was found where the
mother's transfusion was given almost a decade prior to conception. Id. at 871; see Vik
Ed Stoll, Note, PreconceptionTort-The Need for a Limitation, 44 Mo. L. REv. 143 (1979).
Because many employers provide medical care for their employees, this scenario could
also arise in a workplace context leading to employer liability.
71. Cushing v. Time Saver Stores, Inc., 552 So. 2d 730 (La. Ct. App. 1989)
(negligence action by employee's child against employer who forced mother to sit on
stacked boxes in place of office furniture; the boxes shifted, the mother fell, and an
adding machine landed on her abdomen, causing abruptio placenta, which resulted in
birth defects including brain damage); Vicknair v. Hibernia Bldg. Corp., 482 So. 2d 95
(La. Ct. App. 1986) (personal injury action by parents and child of woman who was born
with hyaline membrane disease attributable to mother's running down 21 flights of
stairs in response to a false fire alarm).
72. Fulford v. 1IT Rayonier, Inc., 676 F. Supp. 252 (S.D. Ga. 1987) (wrongful death
action by parents of twin girls who died shortly after premature birth precipitated by
mother's workplace duties that included heavy lifting and pushing wheelbarrows);
Adams v. Denny's Inc., 464 So. 2d 876 (La. Ct. App. 1985) (wrongful death action
against waitress' employer where on-the-job fall caused the death of her unborn child);
Witty v. American Gen. Capital Distributors, Inc., 697 S.W.2d. 636 (Tex. Ct. App. 1985)
(wrongful death action by mother who tripped over utility outlet at work, fatally
injuring unborn child), rev'd on other grounds, 727 S.W.2d 503 (Tex. 1987).
73. While many workplace factors may be associated with low birth weight
including exposure to anesthetic agents, and several solvents, the most consistent
associations are with cigarette and alcohol consumption. See, e.g., OTA, supra note 1, at
1.
74. Premature infants and those small for gestational age are prone to difficulty in
regulating body temperature, respiratory distress, necrotizing enterocolitis, inadequate
sucking and swallowing reflexes, apnea, cerebral hemorrhage, meningitis, and other
problems. BERKOW & FLETCHER, supra note 19, at 7.
may share the toxic exposures of the mother through the con-
tamination of her breast milk.7" Moreover, these shared expo-
sures may be followed by long latency 76
periods and result in
disease and lawsuits years after birth.
Thus, parentally-mediated prenatal harm can occur in
many ways, most of which have been tested in the laboratory
and the courts of various jurisdictions. While a surprising vari-
ety of workplace factors are known or suspected to adversely
affect fetal development, what is most alarming is what is not
yet known. Regarding chemicals, for example, a recent General
Accounting Office (GAO) report estimated that information on
reproductive toxicity exists for only five percent of the 104,000
chemicals registered with the Environmental Protection Agency
(EPA).7 7 Thus, there are 98,800 chemicals in use in the United
States for which we have no data upon which to determine
acceptable risk levels. 78 The paucity of scientific data can, of
course, result in unknowing exposures to harmful circum-
stances. Also possible, however, is the situation where legal
action is brought because scientific evidence at the time of the
lawsuit implicates an agent with a prenatal injury but, upon
later investigation, the causal association is refuted. One such
case may be the anticonvulsant Dilantin (phenytoin) upon
which Harbeson v. Parke-Davis, Inc.,79 discussed below, is
based. Studies have revealed that the children of untreated epi-
leptic mothers experience the same types of anomalies attrib-
uted to Dilantin, a finding that tends to refute the causal
association between the drug and these anomalies.8 0
III. COMPENSABLE REPRODUCTIVE OUTCOMES
While the scientific evidence may implicate an agent with

an adverse reproductive outcome and the courts of another
jurisdiction may have recognized it, that association must also
75. WASHINGTON DEP'T OF LABOR AND INDUS., PUB. No. P-413-035-000, WORKPLACE
HAZARDS TO REPRODUCTivE HEALTH 27 (1991) [hereinafter WORKPLACE HAZARDS].
Nonpolar, low molecular weight contaminants such as polyhalogynated biphenyls and
DDT are likely to be excreted via the breast milk.
76. A cogent example are the vaginal malignancies caused among the adult
daughters of women who used Diethylstilbestrol (DES) in pregnancy. Vale Chem. Co. v.
Hartford Accident and Indem. Co., 490 A.2d 896 (Pa. 1985).
77. Federal Government Efforts to Protect Public, Worker Health Criticized at
Hearing,21 O.S.H. Rep. (BNA) 524 (1991).
78. Id.
79. 98 Wash. 2d 460, 656 P.2d 483 (1983).
80. BERKOW & FLETCHER, supra note 19, at 1753.
be cognizable under Washington law to sustain a lawsuit here.

In Washington, both statutory and case law exists to support
causes of action for most adverse reproductive outcomes.
Washington has recognized prenatal injury to a child born
alive as actionable for over thirty years. 8 1 Thus if an employer's
culpable actions injured a viable fetus via the parent(s), the
child could sue once born. Further, in Harbeson v. Parke-Davis,
Inc.,82 a medical malpractice case, the Washington Supreme
Court also recognized the child's right to sue for birth defects
caused by conduct prior to conception.8 3 Damages available to
the child born with birth defects under such a "wrongful life
action" include extraordinary medical and educational
expenses, and other expenses attributable to the disability. 84
In Harbeson, the court also recognized actions for wrongful
birth on behalf of the parents for prenatal negligence resulting
in the birth of malformed children. The court allowed the par-
ents to recover damages including increased medical and other
expenses associated with the birth and rearing of the child as
well as compensation for "emotional injury caused by the birth
86
of the defective child."
Where the injury to the fetus is so severe that it results in
postpartum death, Washington statutory law steps in to provide
remedies. Where such death occurs before the age of majority,
the parents may maintain a wrongful death action for dam-
81. Seattle-First Nat'l Bank v. Rankin, 59 Wash. 2d 288, 367 P.2d 835 (1962)
(recognizing a cause of action where a child was born with brain damage caused by the
physician's failure to treat the mother's anemia during pregnancy).
82. 98 Wash. 2d 460, 656 P.2d 483 (1983).
83. Id. at 477-78, 656 P.2d at 494 (holding that the physician negligently failed to
warn the female patient of teratogenic risk of "dilantin," an anticonvulsant prescribed
for epileptics).
84. Id. at 480, 656 P.2d at 495. The court provided that the costs of extraordinary
care may only be recovered once. Id. If the parents recover the costs incurred during
the child's minority, the child's recovery would be limited to lifetime costs thereafter.
Id.
85. Id. at 476-78, 656 P.2d at 493-94. Although the court relied on sections of
various statutes when determining the standard of care and damages, it stated that this
action was not based on statute but was a common law negligence action. Id. The
parents were deemed to have a right to avoid the birth of children with congenital
defects, a right the physicians had a duty to protect. Id. at 476, 656 P.2d at 493. The
physicians negligently breached that duty by failing to apprise the parents of the risk of
birth defects due to the mother's anticonvulsant medication. Id. at 477-78, 656 P.2d at
493-94.
86. Id. at 475, 656 P.2d at 493.
ages. 7 Where death occurs later in life, 8 the child's estate or

dependents may file a wrongful death 9 or survival action. 90
Examples of occupational parental exposures that could result
in the later death of offspring are transplacental carcinogens
91 92
such as vinyl chloride and benzene.
In cases of miscarriage due to prenatal injury, Washington
has joined most states 93 in recognizing a viable fetus as a per-
son for purposes of applying the Washington wrongful death
statute, Revised Code of Washington (RCW) 4.24.010.1 4 How-
ever, in Moen v. Hanson,95 the court expressly reserved the
issue of whether such actions could be brought for the death of a
nonviable fetus. 96 The court also refused to establish a bright
line demarcation of fetal viability, leaving that to the finder of
fact at trial.9 7
Wrongful death actions respecting the preborn loom as the
most onerous source of liability facing employers. As illustrated
in Part II, miscarriage and stillbirth are by far the most com-
87. WASH. REV. CODE § 4.24.010 (1992). Section 4.24.010 grants an action by the
natural parents for injury or death of a child. Id. Damages include all expenses
associated with the care of the child as well as loss of love and companionship,
destruction of the parent-child relationship, and other damages as "may be just." Id.
88. Ordinarily, an employment-related prenatal injury action would be tolled
during the injured child's minority. Id. § 4.16.190. Thus, a negligence cause of action,
assuming it were known, would not accrue until age 21. In the case of transplacental
carcinogens, death may not ensue until later in life because of long latency periods.
89. Id. § 4.20.010. Section 4.20.020 specifies the beneficiaries to include the direct
family including spouse, children, grandchildren, and, if none exist, then dependent
parents or siblings. Id. § 4.20.020. No limitation on damages is set.
90. Id. § 4.20.046. Section 4.20.046 grants a survival cause of action to the
deceased's estate for all damages except pain, suffering, anxiety, emotional distress, or
humiliation personal to and suffered by the deceased. Id.
91. See WORKPLACE HAZARDs, supra note 75, at 8.
92. See McDiarmid et al., supra note 57, at 457; see also Savitz & Chen, supra note
15, at 325 (correlating various parental occupations with increased incidence of various
childhood cancers).
93. Sheldon R. Shapiro, Annotation, Right to Maintain Action or to Recover
Damagesfor Death of Unborn Child, 84 A.L.R.3d 411, 422 (1978 & Supp. 1993). Of the
states that have ruled on the issue, 34 have recognized a wrongful death cause of action
based on the death of a viable fetus and 10 have refused to allow such actions,
regardless of viability. Id. Michigan, Louisiana, and Rhode Island have recognized the
action regardless of viability, while Georgia requires that the fetus be quick. Id. Many
states, such as Washington, have not expressly ruled on the issue of viability. Id.
94. WASH. REV. CODE § 4.24.010 (1992).
95. 85 Wash. 2d 597, 537 P.2d 266 (1975) (alleging wrongful death under RCW
4.24.010 based on the death of a fetus when the mother was killed in an automobile
collision during the 8th month of pregnancy).
96. Id. at 601, 537 P.2d at 268.
97. Id. at 601-02, 537 P.2d at 268.
mon and obvious endpoints of developmental harm.9" In fact,

virtually no employment exists that does not involve at least
one factor correlated by at least one researcher with an
increased risk of miscarriage. 99
IV. THEORIES OF LIABiLITY
Assuming the law recognizes the compensability of an

adverse reproductive outcome, it must also provide a basis for
employer culpability. In Washington, strict and negligence the-
ories of liability are possible.
A. Strict Liability
Liability without fault may lie where (1) the employer's
business is deemed an ultrahazardous activity, (2) it poses a
substantial risk of harm no matter how much care is exercised,
and (3) it is not a common activity in the community. 10 0 Possi-
ble workplace scenarios that might result in strict employer lia-
bility for fetal injury include higher risk operations such as
hazardous waste responders, asbestos abatement, fire fighting,
and other jobs where significant risks of exposure are not under
perfect control and where the use of stressful personal protec-
tive equipment is necessary. 01 '
Finally, where the injury is caused by a consumer product,
the Washington Product Liability Act 10 2 may apply where the
employee was exposed to the employer's products in the same
manner as a member of the public.' 0 3
98. Because most germ cell mutations result in early fetal death in test animals, it
would seem reasonable to assume that an employee's exposure to a mutagenic stressor
could result in miscarriage. See CASARETT & DouLL, supra note 29, at 314. There are
thousands of known mutagens in the work environment. U. S. DEP'T OF HEALTH &
HUMAN SERVS., REGISTRY OF Toxic EFFECTS OF CHEMICAL SUBSTANCES (RTECS) (1990)
(listing over 3000 substances that have elicited mutagenesis as well as over 900 that
have caused teratogenesis).
99. In fact, the act of working alone may increase the rate of miscarriage in many
jobs. See, e.g., Agnew et al., supra note 51, at 48 (reviewing literature that shows an
increased risk of miscarriage associated with standing and performing tiring jobs).
100. Klein v. Pyrodine Corp., 117 Wash. 2d 1, 5, 810 P.2d 917, 919 (1991).
101. The use of personal protective equipment such as self-contained breathing
apparatus and limited permeability or heat resistive garments can quickly elevate core
body temperatures resulting in well-documented fetal risk. Agnew et al., supra note 51,
at 436-37.
102. WASH. REV. CODE § 7.72 (1992).
103. Id. § 7.72.030(1). Although the statute expressly states that liability for
design defects or inadequate warnings is predicated on a finding of negligence, the
courts have interpreted this requirement rather loosely. See, e.g., Ayers v. Johnson &
Johnson, 59 Wash. App. 287, 797 P.2d 527 (1990). In Ayers, the court noted that
B. Negligence
Since relatively few occupational exposures are likely to
meet the requirements of strict liability, most actions are likely
to proceed under a negligence theory. A negligence action
would aver that the employer had a duty to the unborn child or
parents, the 4breach of which proximately caused the compensa-
10
ble injury.
1. Duty
In Seattle-FirstNational Bank v. Rankin,10 the Washing-
ton Supreme Court held that when a physician negligently
failed to diagnose and treat a mother's anemia and such anemia
was a proximate cause of injury to the fetus, a personal injury
cause of action arose in the live-born fetus. 10 6 While the court
did not analyze the issue expressly, by implication it found the
10 7
duty to the mother to be a source of a duty owed to the child.
The court later spelled out the duty owed to the unborn child by
physicians or others in Harbeson:
[A] duty may extend to persons not yet conceived at the time
of the negligent act or omission. Such a duty is limited, like
any other duty, by the element of foreseeability. A provider
of health care, or anyone else, will be liable only to those per-
sons foreseeably endangered by his conduct. l '
While the presence of a duty is normally a question of law, 10 9
the determination of the exact bounds of foreseeability is a
question of fact for the jury unless "reasonable minds cannot
differ."1 10
The scope of the employer's duty to protect against prenatal
harm will turn on the foreseeability of such harm as a result of
workplace hazards. Clearly, if the employer knows of the harm-
"foreseeability is not an element of a strict liability claim. Confusion caused by

legislative tinkering should have been erased by now; liability under RCW
7.72.030(1)(a) and (b) rests on traditional strict liability principles in which the concept
of negligence plays no part." Id. at 294, 797 P.2d at 531 (citations omitted).
104. Harbeson v. Parke-Davis, Inc., 98 Wash. 2d 460, 468, 656 P.2d 483, 489
(1983).
105. 59 Wash. 2d 288, 367 P.2d 835 (1962).
106. Id. at 291, 367 P.2d at 838.
107. Id.
108. Harbeson, 98 Wash. 2d at 480, 656 P.2d at 489 (citation omitted) (emphasis
added).
109. Hansen v. Friend, 118 Wash. 2d 476, 479, 824 P.2d 483, 485 (1992).
110. Christen v. Lee, 113 Wash. 2d 479, 492, 780 P.2d 1307, 1313 (1989).
ful effects of a workplace hazard and an employee's susceptibil-

ity to that hazard, the duty will be established. The question
remains, however, whether the average employer will be
charged, as were the physicians in Harbeson,with the responsi-
bility of continually researching the literature to ascertain
obscure or newly-recognized prenatal hazards."' While no
cases on the issue exist, the answer is probably yes. Under the
Washington Industrial Safety and Health Act of 1973
(WISHA), 1 1 2 the employer is charged with maintaining the
workplace "free from recognized hazards that are causing or
likely to cause serious injury or death to his employees." 1 3 By
implication, the employer is charged with doing the research
necessary to know of those hazards." 4 Additionally, regula-
tions promulgated under WISHA expressly recognize "repro-
ductive toxins" as occupational health hazards."' 5 Because
most of the literature respecting reproductive hazards to the
employees also includes prenatal hazard information, an
employer would likely be charged with constructive knowledge
1 16
of both.
The duty to protect against prenatal harm does not end
with the employer. Individual co-employees, consultants, con-
tractors, and others who bear responsibility for managing work-
place risks, as well as manufacturers and suppliers of
chemicals, equipment, and other instrumentalities of prenatal
111. Harbeson, 98 Wash. 2d at 476, 656 P.2d at 493.

112. WAsH. REv. CODE § 49.17 (1992).
113. Id. at § 49.17.060 (emphasis added).
114. RCW 49.17.180(6) requires employers to exercise "reasonable diligence" to
discover violations of WISHA standards. WASH. REV. CODE § 49.17.180(6) (1992). The
Division of Industrial Safety and Health states that "as a general rule, if the (safety and
health] inspector was able to discover a violation, he/she can presume that an employer
could have discovered the same condition through the exercise of reasonable diligence."
DIvISION OF INDUS. SAFETY & HEALTH, DEP'T OF LABOR & INDUS., WISHA OPERATIONS
MANUAL ch. VIII (1985).
115. See WASH. ADMiN. CODE § 296-62-05405(21) (1992); see also id. § 296-62-
05043. WISHA duties under specific regulations extend to all workers on an employer's
job site, including those of independent contractors. Stute v. P.B.M.C., Inc., 114 Wash.
2d 454, 457, 788 P.2d 545, 547 (1990).
116. Implicit in the employers duty to become familiar with prenatal hazards to the
employees may be the duty to know of the reproductive status of those employees. This
may be impeded by regulatory prohibitions such as Washington Administrative Code
(WAC) 162-12-140. WASH. ADMiN. CODE § 162-12-140 (1992). Section 162-12-140
defines "[aill questions as to pregnancy, and medical history concerning pregnancy and
related matters" as unfair preemployment inquiries. Id. WISHA deals with the issue in
a gingerly manner in its lead standard by mandating pregnancy testing if the employee
requests it. Id. § 296-62-07521(11)(c)(ii)(F).
injury, may also face liability. 11 7 For co-employees, this liability

can be particularly onerous because they may no longer be
employed or indemnified by the employer at the time of the law-
suit. 118 In addition, because statutory time limitations may be
tolled for many years or, in preconception cases, generations, co-
employees (or their estates) may be the only parties remaining
to be sued if the employer's business has been dissolved.
2. Breach
The regulations promulgated under WISHA also serve as a
baseline for determining the standard of care in discharging an
employer's duty."19 Under the WISHA hazard communication
provision, the employer would have a duty to warn of such
hazards. 20 Likewise, the employer would be bound to adhere
to specific WISHA safety standards for exposures of employees.
The duty to protect beyond mere compliance with WISHA
safety regulations would be determined on a case-by-case basis
in light of traditional negligence factors such as the probability
and gravity of the harm balanced against the feasibility and
121
cost of risk-reducing measures.
117. See, e.g., Namislo v. AKZO Chem., Inc., 620 So. 2d 573 (Ala. 1993) (complaint
included claims for fraud, outrage, and willful conduct against co-employees); Cushing
v. Time Saver Stores, Inc., 552 So. 2d 730 (La. Ct. App. 1989) (complaint included a
claim against a supervisor for negligent supervision and failure to provide a safe
workplace).
118. The employer who has been sued may name a current or former co-employee
as a codefendant or may seek contribution or indemnification. See WASH. REv. CODE
§ 4.22.040 (1992) (Washington's general contributory fault and indemnification statute).
119. Doss v. ITT Rayonier, Inc., 60 Wash. App. 125, 129-30, 803 P.2d 4, 7 (holding
that WISHA statutes are admissible as evidence of the standard of care in negligence
actions), review denied, 116 Wash. 2d 1034, 813 P.2d 583 (1991).
120. WASH. ADMIN. CODE § 296-62 (1992). WAC 296-62 enunciates a lengthy list of
employer responsibilities respecting the gathering and dissemination of workplace
hazard information. Id. The focus of the standard is on "chemicals" and does not
include "intangible" exposures or "safety' hazards. Id. The requirement of WAC 296-
24-073(2) that the employer "do every other thing necessary to protect the life and
safety of employees" could fill this gap. Id. § 296-24-073(2).
121. Because of inadequate data and the delay in the promulgation of safety and
health regulations, most workplace standards do not contemplate prenatal harm. See
OTA, supra note 1, at 1, 9-10, 60. Thus, employers who merely comply with applicable
WISHA regulations do so at their own peril. Lead exposure is a good example. The
current WISHA standard allows blood lead levels as high as 50 micrograms per deciliter
of blood (ug/dl). WASH. ADMIN. CODE § 296-62-07521(12)(a)(i)(D) (1992). Meanwhile,
the American Conference of Governmental Industrial Hygienists (ACGIH) has adopted
a 20 ug/dl standard to prevent prenatal cognitive developmental harm. Note, ACGIH
ConsideringAdopting Limit for Blood Levels ofExposed Workers, 23 O.S.H. Rep. (BNA)
6 (1993). The scientific community, however, is far from certain that even the ACGIH
levels are safe. See, e.g., Ellen K Silberg, Implicationsof New Data on Lead Toxicity for
Conflicting policy considerations make the task of defining

due care problematic in prenatal injury cases. Such problems
start with the very definition of safety. In the parlance of safety
and health regulation, "safe" means that level of exposure for
which the risk of death or disability is not deemed signifi-
cant. 1 22 In tort litigation, however, that same risk may result in
culpability if it is deemed unreasonable in the particular case.
Thus, it is unlikely that mere compliance with WISHA regula-
tions will allow an employer to escape tort negligence liability
for injury to the unborn child of an employee.' 2 3
There are, of course, other consensus safety standards that
often are more risk averse than those of regulators such as
WISHA.' 2 4 Even those standards, however, can serve as no
Managing and Preventing Exposure, 89 ENVTL. HEALTH PERsP. 110 (1990) ("Current
biomedical consensus accepts that blood lead levels as low as 5 to 15 ug/di are risky to
fetuses, young children, and adults.").
122. See Industrial Union Dep't v. American Petroleum Inst., 448 U.S. 607, 642
(1980) (stating that "'safe' is not the equivalent of 'risk-free'" and that the statutory
mandate of the Occupational Safety and Health Administration (OSHA) was to be
limited to the control of significant occupational risks only). This decision has been
interpreted by OSHA to allow an asbestos-related cancer mortality risk of 6.7 deaths
per 1000 workers over a lifetime. 51 Fed. Reg. 22,647 (1986). In the case of agents that
are carcinogenic or mutagenic, policy decisions respecting risk are generally based on
the assumption that there is no level of exposure that is risk free. See, e.g., 29 C.F.R.
§ 1990.111 (1992). Thus "safety" is defined as that statistical probability of cancer that
is deemed acceptable under the circumstances. With noncarcinogens (including most
fetotoxic or teratogenic stressors), safety limits tend to represent the level of exposure
below which the body is able to resist or repair damage or for which the effect of
exposure is not deemed to result in a "material impairment of health or functional
capacity." 54 Fed. Reg. 2361 (1989). Because of interpersonal variations in
susceptibility, however, there will always be some proportion of the population who will
experience disability at levels below the safety standards. A good example is the
exposure limit for noise. Exposure at the legal limit is known to protect only 85% to
90% of the population from compensable hearing loss. It is, as a practical matter,
impossible to set exposure levels for most occupational health hazards that are risk free.
The best that can be hoped for is low risk. See WILLIAM W. LOWRANCE, OF ACCEPTABLE
RisK 11 (1976).
123. While the balance of various broad policy interests may restrict regulators in
the management of occupational risks to employees, the courts are not similarly
restricted in civil suits. It has been held that risks far below one in a thousand may form
the basis for liability. See, e.g., Davis v. Wyeth Labs., Inc., 399 F.2d 121, 129-30 (9th
Cir. 1968) (holding that the failure to warn of a one in a million risk of polio from a
vaccine rendered defendant liable); see also Ayers v. Johnson & Johnson, 59 Wash. App.
287, 297, 797 P.2d 527, 553 (1990) (finding liability for the failure to warn of the risk of
aspirating baby oil in spite of the company having sold over 500 million bottles of the
product without a single reported case of aspiration).
124. The major standard-setting body respecting occupational health hazards is
the American Conference of Governmental Industrial Hygienists (Lansing, Michigan).
Their consensus standards formed the basis of the original standards promulgated
under the federal Occupational Safety and Health Act of 1970. Occupational Safety and
19941 PrenatalHarm in the Workplace 301
more than evidence of the requisite standard of care, leaving

compliant employers with a lingering doubt as to future
liability.
Irrespective of the care taken by an employer, the plaintiff
is likely to present expert testimony at trial to establish that
more protective efforts were possible. 25 The employer will then
have to justify its reasons for not making those efforts in cases
where the jury is presented with a child who may not have been
injured if the employer had spent a few more dollars.
3. Causation
Some commentators have argued that prenatal injury suits
are difficult to prove because of the lack of extensive data on
prenatal hazards and the inability to definitively point to a par-
ticular chemical as the cause of an injury. 126 It is true that very
few suits have been filed to date and that most of those have
alleged traumatic injury or exposure to acute toxins such as car-
bon monoxide.1 27 A more appropriate analysis, however, should
focus on how such cases will be treated when they are
pursued.128
With respect to obscure, tenuous associations, Washington
courts have been fairly generous to plaintiffs in prenatal injury
litigation to date. In Rankin, the court noted that "[wie are not
Health Act of 1970, Pub. L. No. 91-596, 84 Stat. 1590 (codified at 29 U.S.C. §§ 651-678
(1988)). These standards are updated yearly to reflect changes in the science. Because
they are not hampered by administrative procedures requiring notice or comment, the
standards tend to be more responsive to contemporary scientific research.
125. Even if an exposure has not been definitively determined to pose a prenatal
hazard, entrepreneurs are capitalizing on concerns about safety and developing safe
alternatives. See, e.g., Radiation-FreeComputer Monitor Introduced; Said To Avoid
Potential Miscarriage Problems, 18 O.S.H. Rep. (BNA) 1888 (1989) (advertising
"Radiation-free" video display monitor expected to "prevent miscarriages and other
reproductive problems").
126. See, e.g., Williams, supra note 4, at 646 n.25 ("Indeed, the problems of proving
causation may be so great that professed employer concern about liability may be a
pretext for sex discrimination.").
127. Acute causes of occupational injury also receive disproportionate
representation in the workers' compensation arena. This may be because many
occupational diseases are not recognized as such by employees. See, e.g., Elinar P.
Schroeder & Sidney A. Shapiro, Responses to Occupational Disease: The Role of
Markets, Regulation, and Information, 72 GEO. L.J. 1231, 1245 (1984) (noting that only
2% to 3% of workers' compensation payments are for occupational diseases while 97% of
those afflicted with serious occupational diseases are not compensated at all).
128. In light of the increasing awareness of new and varied cause-and-effect
relationships, an increasing number of attorneys joining the field, and the recent
expansion of the rights of the unborn, it should be assumed that more and more
plaintiffs will be seeking redress in the future.
unmindful of the fact that a claim for prenatal injuries is prone

to present difficult causation issues. This, however, is no rea-
son to deny the sufficiency of the pleading. Difficulty of proof
does not prevent the assertion of a legal right."' 2 9 The court
went on to hold that liability could be found on the basis of testi-
mony that the incremental loss in the mother's oxygen-carrying
ability due to an undiagnosed anemia could compound the effect
of her blood loss during delivery and ultimately cause cerebral
palsy in her child.130 In Harbeson,the court upheld a finding of
causation of a child's "fetal hydantoin syndrome" on the basis of
epidemiological studies in the literature that showed an
increased incidence of the syndrome among users of the pre-
13 1
scription drug used by the mother.
Other jurisdictions have also been very reluctant to take
prenatal injury cases away from a jury on the basis of tenuous
causation evidence, preferring to leave the issue to a battle of
the experts. 1 3 2 As in Harbeson, much of that battle has turned
on epidemiological studies. 13 3 The court in Ferebee v. Chevron
Chemical, Co. 13 4 made the following observation:
Judges, both trial and appellate, have no special competence
to resolve the complex and refractory causal issues raised by
the attempt to link low level exposure to toxic chemicals with
human disease. On questions such as these, which stand at
the frontier of current medical and epidemiological inquiry, if
experts are willing to testify that such a link exists,135it is for
the jury to decide whether to credit such testimony.
In Wells v. Ortho PharmaceuticalCorp.,136 the court held that
liability for failure to warn could arise "as soon as there was a
129. Seattle-First Nat'l Bank v. Rankin, 59 Wash. 2d 288, 292, 367 P.2d 835, 383
(1962).
130. Id. at 293, 367 P.2d at 838.
131. Harbeson v. Parke-Davis, Inc., 98 Wash. 2d 460, 477, 656 P.2d 483, 493-94
(1983). Subsequent research has refuted the association, finding that similar birth
defects occur among the children of untreated epileptics. BERKOW & FLETCHER, supra
note 19, at 1753.
132. See, e.g., Wells v. Ortho Pharmaceutical Corp., 788 F.2d 741, 744-45 (11th.
Cir. 1986).
133. Harbeson, 98 Wash. 2d at 477, 656 P.2d at 493-94; see also Oxendine v.
Merrell Dow Pharmaceuticals, Inc., 506 A.2d 1100 (D.C. 1986). Of note in Oxendine is
the fact that none of the epidemiological studies relied on by the plaintiffs showed a
statistically-significant association of birth defects with the defendant's product. Id. at
1107-09.
134. 736 F.2d 1529 (D.C. Cir. 1984).
135. Id. at 1534.
136. 615 F. Supp. 262 (N.D. Ga. 1985).
hint of a possibility that the [spermicide] causes birth

defects."' 3 7 Application of the Wells hint-of-a-possibility test to
the array of epidemiological and toxicological studies already in
existence would probably yield lawsuits for prenatal injury by
employees in thousands of occupations.
A coup de grace to the notion that a scientific consensus
must support the casual association between an alleged expo-
sure and a fetal injury was delivered by the U.S. Supreme Court
in Daubert v. Merrel Dow Pharmaceutical,Inc.13 8 In that case,
the Court ruled that plaintiffs' experts could testify as to a
drug's teratogenicity on the basis of their own reanalyses of the
data in peer-reviewed epidemiologic studies that refuted such
association. 1 39 This rejection of the test adopted in Frye v.
U.S.140 opens the door to anyone who can qualify as an expert
and opine in plaintiffs favor, so long as the scientific method
underlies the expert's reasoning.' 4 '
Another causation issue concerns indirect injury. Many
exposures in the workplace, as well as personal habits such as
smoking and nutrition, result in the birth of babies that are
preterm or small for their gestational age. These conditions,
while not injuries in the strictest sense of the term, do predis-
pose babies to illness and death.'42 While Washington courts
have not ruled on this scenario, the Court of Appeals for the
Fifth Circuit has. Applying Louisiana law, the court said that if
an infant's right "to the start in life that results from nature's
scheme of granting a nine months' period of gestation" is inter-
fered with by the negligence of another, and if it is shown that
such interference substantially increased the chances of death
from an outcome that actually did cause death, then the jury
could attribute the death to the negligent act that caused the
premature birth. 4 3 In light of the holdings in Rankin and Har-
beson, it is likely that Washington courts would adopt a similar
position.
Most workplace fetal injury lawsuits to date have involved
well known prenatal hazards such as trauma, rubella, or hyp-
137. Id. at 294.

138. 113 S. Ct. 2786 (1993).
139. Id. at 2792, 2799.
140. 293 F.2d 1013 (D.C. Cir. 1923) (holding that scientific evidence must attain
general acceptance in the professional community before it may be admitted at trial).
141. Daubert, 113 S. Ct. at 2795.
142. See BERKOW & FULTcHER, supra note 19, at 1853-54, 1856.
143. Pan-American Casualty v. Reed, 240 F.2d 336, 340 (5th Cir. 1957).
oxia. In such cases, the question of causation is relatively

straightforward. 4 4 However, actions involving more insidious
1 45
workplace fetal hazards are also beginning to be reported.
4. Damages
Although the types of damages allowable in Washington

have been discussed earlier in this Article, 46 the potential judg-
ment amounts also deserve discussion. Tort damage awards for
prenatal injuries in the workplace are not governed by the lim-
its that apply to workers' compensation claims nor are they paid
out over years as are disability pensions.' 4 7 They are left to the
jury and are payable at once.
The Washington cases involving childhood injuries have
been telling. In Rankin, the jury awarded $89,000 in 1962 to a
child who suffered cerebral palsy due to anoxia caused by her
mother's untreated anemia. 48 In Ayers v. Johnson & John-
son,' 4 9 a product liability action, the jury awarded $500,000 to
the parents and $2,000,000 to the child who suffered cardiac
arrest leading to paralysis, mental retardation, and seizures
due to aspiration of baby oil. 15 0 In contrast, under industrial
insurance, an employee's permanently and totally disabling
144. See BERKOW & FLETCHER, supra note 19, at 1871, 1875, 1911.
145. Of the dozen workplace prenatal injury lawsuits cited in this Article, the
alleged causation included the following: Thompson v. Pizza Hut of America, Inc., 767
F. Supp. 916 (N.D. Ill. 1991) (plaintiff inhaled carbon monoxide during office renovation
in 1st trimester); Fulford v. ITT Rayonier, Inc., 676 F. Supp. 252 (S.D. Ga. 1987)
(plaintiff had to push a wheelbarrow); Namislo v. AKZO Chem., Inc., 620 So. 2d 573
(Ala. 1973) (mother exposed to mercury); Bell v. Macys, 261 Cal. Rptr. 455, 447 (Ct.
App. 1989) (plaintiff was negligently treated by company nurse during labor); Cushing
v. Time Saver Stores, Inc., 552 So. 2d 730 (La. Ct. App. 1989) (adding machine fell on
plaintiffs abdomen); Vicknair v. Hibernia Bldg. Corp., 482 So. 2d 95 (La. Ct. App. 1986)
(plaintiff ran down stairs); Adams v. Denny's Inc., 464 So. 2d 876 (La. Ct. App. 1985)
(plaintiff tripped and fell in restaurant); Jarvis v. Providence Hosp., 444 N.W.2d 236
(Mich. Ct. App. 1989) (plaintiff inhaled carbon monoxide because of leak from furnace
and contracted hepatitis); Dillon v. S. S. Kresge, 192 N.W.2d 661 (Mich. Ct. App. 1971)
(plaintiff contracted rubella); Stelly v. Firestone Tire & Rubber Co., 20 O.S.H. Rep.
(BNA) 1040 (Tex. Dist. Ct. Oct. 21, 1990) (father exposed to mercury); Witty v.
American Gen. Capital Distrib., Inc., 697 S.W.2d 636 (Tex. Ct. App. 1985) (plaintiff
tripped over utility outlet and fell), rev'd on other grounds, 727 S.W.2d 636 (Tex. 1987).
146. See discussion supra part III.
147. WASH. REv. CODE § 51.32.010 (1992). RCW 51.32.010 limits eligibility to
workers injured within the course of employment. Id.
148. Seattle-First Nat'l Bank v. Rankin, 59 Wash. 2d 288, 291, 367 P.2d 835, 837
(1992). At 5% inflation, $89,000 in 1962 is equivalent to $404,000 in 1993.
149. 59 Wash. App. 287, 797 P.2d 527 (1990).
150. Id. at 289, 797 P.2d at 529.
occupational impairment is compensated by monthly payments

at or below the average monthly wage in the state.1 5 '
Other jurisdictions have yielded large verdicts in prenatal
injury cases. In Wells v. Ortho PharmaceuticalCorp., the plain-
tiff was awarded $5.1 million for birth defects caused by spermi-
cidal jelly, including the lack of a left arm, an under-developed
left shoulder, a cleft lip, a nostril deformity, and an optic nerve
defect in one eye.'" 2
Such large isolated damage awards are likely to be intimi-
dating to future defendants. Although some cases will be
decided in favor of defendants, it will be the stalwart employer
who will refuse to settle when faced with a prenatal injury case
that cannot be dismissed on motion before trial. 5 3 The unpre-
dictability of damage awards is also likely to lead liability insur-
ance carriers to attempt to exclude such risks in the future.
The aggregate cost to industry is potentially overwhelming
if a cause of action for previability fetal death (miscarriage)
gains acceptance. Because the background rate of recognized
miscarriage is approximately fifteen percent,15 4 a two or three-
fold increase in that rate in a particular occupation could mean
that fifteen to thirty percent of all conceptions in that popula-
tion result in a prima facie wrongful death action.'15 To date,
only Louisiana, 5 6 Michigan, 5 7 and Rhode Island15 8 would per-
mit a wrongful death action based on the death of a nonviable
151. WASH. REV. CODE § 51.32.060 (1992). Different compensation is afforded to

employees based on marital status and number of children. Provision is also made to
pay for a full time attendant if the worker is rendered "physically helpless." Id.
152. 788 F.2d 741, 743 (11th Cir. 1986). In the district court's breakdown of the
award, $3,000,000 was apportioned to compensate for the child's past pain and suffering
and $500,000 for the mother's mental distress. Id. The balance covered past and
present pecuniary losses of mother and child. Id.
153. See, e.g., Stelly v. Firestone Tire & Rubber Co., 20 O.S.H. Rep. (BNA) 1040
(Tex. Dist. Ct. Oct. 21, 1990) (awarding a structured settlement including compensation
for the child worth $6.25 million).
154. While the true miscarriage rate is 43%, a large percentage of these occur prior
to detection and confirmation of pregnancy. The rates reported for purposes of
epidemiological studies vary with different populations but range from about 10% to
15%. OTA, supra note 1.
155. For an individual employer, miscarriage clusters could be catastrophic. See,
e.g., Note, 18 O.S.H. Rep. (BNA) 1700 (noting a cluster of 14 miscarriages among 11
women in one year in a company whose drinking fountains were later found to contain
3.5 times the acceptable level of lead).
156. Adams v. Denny's Inc., 464 So. 2d 876 (La. Ct. App. 1985) (recognizing that a
"human being exists from the moment of fertilization and implantation").
157. Fryover v. Forbes, 439 N.W.2d 284 (Mich. Ct. App. 1989).
158. Presley v. Newport Hosp., 365 A.2d 748, 754 (R.I. 1976).
fetus, while Georgia would permit such an action after the fetus
1 59
became quick.
If such actions were to extend to the moment of conception
(as in Louisiana) and science advances to the point where it can
reliably detect the estimated forty percent of abortions that
occur in the first couple of weeks following conception, the num-
16
bers of such lawsuits could skyrocket. 1
V. DEFENSES TO EMPLOYER LIABILITY
In most workplace injury scenarios, employers may invoke

certain defenses to liability. These defenses may be based on
statutory immunity, intervening forces, or the conduct of the
plaintiff. In the case of prenatal hazards, however, these
defenses are compromised.
A. Workers' Compensation Exclusivity

The quid pro quo of workers' compensation is that the
employer will pay or insure for scheduled compensation to
employees injured on the job in exchange for immunity from
tort liability.1 6 ' This immunity applies to
62
co-employees and to
contractors providing personal services.1
Washington courts have not directly ruled on the issue of
whether RCW 51.24163 bars prenatal injury actions attributable
to the parent's workplace. The issue turns on the determina-
tion of whether prenatal injury to the offspring constitutes
injury to the employee/parent.
Most of the jurisdictions that have considered the issue
have not barred actions based on injury or death of the fetus. In
Witty v. American General Capital Distributors, Inc.,' 64 the
159. Porter v. Lassiter, 87 S.E.2d 100, 103 (Ga. Ct. App. 1955). When the fetus
becomes quick is a question for the jury. Id. In this case, the plaintiff miscarried in the
5th month. Id. at 102.
161. WASH. REV. CODE §§ 51.24.020-.902 (1992).
162. Kerr v. Olson, 59 Wash. App. 470, 477, 798 P.2d 819, 822 (1990) (holding that
contractor physicians who worked in employer's clinic are also entitled to immunity).
The immunity of federal co-employees is based on the determination of whether they
are performing discretionary functions and the exclusive remedy provision of the state
law that governs the lawsuits. Andrews v. Benson, 809 F.2d 1537 (11th Cir. 1987).,
Safety engineers have been held to be performing nondiscretionary duties and to not be
protected by sovereign immunity. Id.
163. WASH. REv. CODE § 51.24 (1992).
164. 697 S.W.2d 636 (Tex. App. 1985), rev'd on othergrounds, 727 S.W.2d 503 (Tex.
1987).
Texas Court of Appeals ruled that the workers' compensation

exclusive remedy provision barred a mother's claim for emo-
tional distress but not a wrongful death claim. 16 5 In Thompson
v. Pizza Hut of America,'6 6 the Illinois' workers' compensation
statute was interpreted to allow an action by an infant born
with neurological damage due to its mother's workplace expo-
sure. 1 6 7 In Cushing v. Time Saver Stores,168 a Louisiana court
noted that the "Louisiana Workers' Compensation Act was
neither intended nor purports to affect the rights of an
employee's child who is injured on the employee's job site."' 6 9
The court went on to allow the child's claim for brain damage 70
caused by the mother's workplace trauma during pregnancy.
Michigan has also refused to interpose exclusivity in prenatal
injury actions. For example, in Jarvis v. Providence Hospi-
tal,' 7 1 the court noted the potential burden on employers of
pregnant women but determined that "[a]ny decision to extend
the exclusive remedy provision of the Workers' Disability Com-
pensation Act to limit the protection given to fetuses must be
made by the Legislature."' 7 2 Alabama'" and Tennessee 7 4
have also refused to bar actions based on the injury or death of
an employee's offspring.
Only California has reached a different result. In barring
wrongful death and survival actions based on the death of an
employee's child, the court in Bell v. Macy's California1 75 said
that to hold otherwise would result in "adverse consequences to
female employees, who could easily find themselves the victims
of financially driven gender discrimination by liability conscious
employers." 7 6 The court reasoned that the fetal injury was
165. Id. at 640; see also Stelly v. Firestone Tire & Rubber Co., 20 O.S.H. Rep.
(BNA) 1040 (Tex. Dist. Ct. Oct. 21, 1990).
166. 767 F. Supp. 916 (N.D. Ill. 1991).
167. Id. at 919.
168. 552 So. 2d 730 (La. Ct. App. 1989).
169. Id. at 732; see also Adams v. Denny's Inc., 464 So. 2d 876 (La. Ct. App. 1985)
(holding that parents' wrongful death claim for miscarriage due to fall at work is not
barred). In Cushing, the court analogized to the case where the employee brought her
child to work and the child was injured and killed because of the employer's negligence.
Cushing, 552 So. 2d at 732.
170. Cushing, 552 So. 2d at 732.
171. 444 N.W.2d 236 (Mich. Ct. App. 1989).
172. Id. at 291.
173. See Namislo v. AZKO Chem., Inc., 620 So. 2d 573, 575 (Ala. 1973).
174. Brewer v. Monsanto Corp., 644 F. Supp. 1267, 1274 (M.D. Tenn. 1986).
175. 261 Cal. Rptr. 455 (Ct. App. 1989).
176. Id. at 447. The court likened in utero injuries via the mother to loss of
consortium cases where the family of the employee is injured by the loss of a family
derivative of injury to the mother and thus barred by the state's

workers' compensation statute. 177 In response, the California
Legislature passed a bill permitting tort actions based on work-
place prenatal injuries but the bill was vetoed by the
78
Governor.
B. Compliance with Title VII

An employer might try to avoid liability by claiming that
federal antidiscrimination laws left it no choice but to expose
the female employees to prenatal risks. The basis for this asser-
tion is found in International Union, UAW v. Johnson Con-
trols,179 where the U.S. Supreme Court held that an employer's
policy of excluding fertile or pregnant women from jobs that
entailed exposure to fetal hazards was impermissible sexual
discrimination under Title VII of the Civil Rights Act of 1964.180
Yet for apprehensive employers, the Court held out the follow-
ing hope:
Without negligence, it would be difficult for a court to find
liability on the part of the employer. If, under general tort
principles, Title VII bans sex-specific fetal-protection policies,
the employer fully informs the woman of the risk, and the
employer has not acted negligently, the8 basis for holding an
employer liable seems remote at best.' 1
The Court went on to say that such liability may be preempted
if state tort law "impede[s]18 the accomplishment of Congress'
2
goals in enacting Title VII."
member or their services. Id. at 454. It also made a comparison with a case barring a
family's claim against an employer for injuries caused by the father who was driven
insane by work. Id. As the dissent pointed out, however, although they were both
injured at the same time, the injury to the fetus did not accrue from an injury to the
mother. Id. at 457.
177. Id. at 454. Applying this tendentious reasoning, the court would, presumably,
bar a personal injury action by children who are injured, along with their mothers, at
work. Thus, an employee who is negligently caused to fall while carrying a child at
work would be compensated but the child would not.
178. See California Civil Rights Act Amendment Sought To Prohibit Pregnant
Workers From Some Jobs, 21 O.S.H. Rep. (BNA) 549 (1991) (noting that as he vetoed
Assembly Bill 489, the Governor called for legislation that would permit employers to
institute fetal protection programs to prevent such harm).
179. 497 U.S. 187 (1991).
180. Id. at 197.
181. Id. at 208.
182. Id. at 209. In response, the concurring opinion pointed out that (1)
preemption of state tort law by Title VII is not supported by precedent, (2) warnings to
employees would not preclude their children's cause of action, and (3) employers cannot
determine in advance what conduct will constitute negligence because compliance with
By invoking Johnson Controls, an employer who has com-

plied with WISHA standards and has apprised its employees of
the risks of prenatal injury in the workplace may try to avoid
liability in the event of prenatal injury. The employer would
contend that, had it not been for Title VII, the employer would
have protected the fetus from injury by removing the mother
from the injurious exposure. However, as was discussed earlier
in this Article,18 3 most prenatal injuries derive from very mun-
dane occupational hazards that are ubiquitous in the work-
place. Thus, assuming, arguendo, that a preemption defense
were valid, an employer seeking to claim the defense would
have to contend that, freed from the restrictions of Title VII, it
would have excluded most women from most jobs. It is doubtful
that such a claim could prevail in most prenatal injury cases.
C. Compliance With Safety Regulations

It is black letter tort law that compliance with regulatory
standards is not a defense to an allegation of negligence."' In
Washington, while evidence of compliance with a standard will
be admissible as evidence of due care, the only circumstance
where compliance with a government mandate will preclude lia-
bility occurs under the Products Liability Act in the case of
products made to government specifications respecting design
or warnings.'8 5 As previously discussed, WISHA standards
entail risks that may exceed those deemed appropriate for fetal
exposures and thus expose the employer to liability.' 8
D. ParentalNegligence
In many cases of prenatal injury, the employer and the
employee may share responsibility. For example, a father who
is exposed to a toxin at work may not adhere to all safety rules
and thereby increase his exposure. A mother may be exposed to
solvents at work while also consuming alcohol at home.' Such
occupational safety and health regulations has been held not to be a defense to state tort
liability. Id. at 211 (White, J., concurring).
183. See supra notes 53-80 and accompanying text.
184. W. PAGE KEETON ET AL., PROSSER AND KEETON ON THE LAw OF TORTS § 36, at
323 (5th ed. 1984).
185. WASH. REv. CODE § 7.72.050 (1992).
186. See supra notes 112-125 and accompanying text.
187. Fetal alcohol syndrome and fetal solvent syndrome manifest themselves in
similar reproductive outcomes. Other factors, notably cigarette consumption, can
magnify the risks from workplace exposures. See OTA, supra note 1, at 60, 82.
behavior may result in different legal outcomes depending on

the claims asserted.
In most cases where the child is born with an injury, paren-
tal misconduct would probably not be attributed to the child to
reduce or defeat recovery. Washington courts have long held
that a parent's negligence will not be imputed to the child in
personal injury actions.18 8 Similarly, in a wrongful death action
based on the death of a child, the negligence of one parent
would not be imputed to the other.' 8 9 The employer may, how-
ever, have a right of contribution against the negligent parent
proportionate to that parent's share of fault. 190
However, in cases where the parental behavior was reck-
less and extreme, a court may determine that such reckless-
ness serves to cut off the causal connection between the
employer's conduct and the child's injury. In Walker v.
Rinck,19 ' for example, the Indiana Court of Appeals held that a
parent's negligent conduct could constitute an intervening,
superseding cause of their child's birth defects.' 92 The parents
knew of the mother's Rh sensitization and of the consequent
risk of fetal harm. 9 3 Yet they proceeded to conceive anyway,
giving birth to three children, all of whom suffered injury."'
The court held that their conduct cut19 5off any liability for prior
negligence by health care providers.
E. ParentalAssumption of Risk
In Washington, "[a] parent does not have legal authority to

waive a child's own future cause of action for personal injuries
resulting from a third party's negligence."' 9 6 Thus, in most
cases, an employer's receipt of parental consent would prove
188. Vioen v. Cluff, 69 Wash. 2d 306, 316, 418 P.2d 430, 437 (1966).
189. WASH. REV. CODE § 4.22.020 (1992).
190. Id. at § 4.22.040.
191. 566 N.E.2d 1088 (Ind. Ct. App. 1991).
192. Id. at 1090.
193. Id.
194. Id.
195. Id. In fact, the parents conceived twice. The first time, the baby was
premature, anemic, and suffered respiratory problems. The second time, they conceived
twins, one of whom suffered birth defects including hearing impairment, motor skills
deficiencies, and possible mental retardation, the other one being asthmatic. Id. at
1089.
196. Scott v. Pacific West Mountain Resort, 119 Wash. 2d 484, 495, 834 P.2d 6, 10
(1992).
ineffective. Similarly, an agreement to waive a future claim

based on strict liability would also fail.' 9 7
The best that an employer might hope to accomplish is a
waiver of the parents' rights in a wrongful death or survival
action. Additionally, an employer could seek indemnification
from the parents concerning injury to the child. However, such
indemnification would only be as valuable as the parents'
resources. Furthermore, such agreements would have to sur-
198
vive court scrutiny respecting public policy.
VI. THE POLICY GoALs OF A SOLUTION
A problem clearly exists. Many prenatal injuries are proba-

bly accruing daily from occupational exposures. Yet very few
victims are receiving compensation through the tort system
because the system is ill-equipped to handle such cases. Never-
theless, the fear of massive, unpredictable tort liability results
in an incentive for employers to exclude fertile and pregnant
women from certain occupations. In addition, the trend is such
that the employers' liability fears may soon come to pass. All
but one of the employment-related prenatal injury cases cited
herein arose within the last ten years.
As several commentators and courts have pointed out, only
legislation can ameliorate this problem.' 99 In crafting such leg-
islation, all affected interests should be accommodated and bal-
anced. First and foremost, for obvious reasons, legislation
should work toward preventing prenatal injury. However, con-
trary to the suggestions of some, the occurrence of prenatal
injuries cannot be eliminated, but merely reduced.2 0 0 Thus, we
must also be prepared to fairly compensate persons whose inju-
ries fall through the cracks in those legislative safeguards, just
as we do for persons who suffer other work-related injuries and
illnesses.
197. Id. at 494, 834 P.2d at 11 ( "Under Washington law parents may not settle or
release a child's claim without prior court approval.").
198. The agreement would be ineffective with respect to gross negligence or where
the terms were unduly oppressive or unfair. In the employment context, it is likely that
most agreements would be presumed unconscionable based on the respective
bargaining power of the parties.
199. See, e.g., Bell v. Macy's California, 261 Cal. Rptr. 455 (Ct. App. 1989).
200. See, e.g., Buss, supra note 4, at 592-96. Buss argues that most prenatal
hazards are attributable to exotic chemicals that should be banned. While there are a
few stressors that can be replaced with functionally-equivalent substitutes, most
prenatal injury is attributable to everyday exposures, which are an inexorable part of
modem civilization.
The incentive to exclude women should also be eliminated.

The ability to bear a child should be considered a gift, not a lia-
bility. Fetal protection policies in isolated industries have gen-
erated some of the most acrimonious debates concerning the
1
workplace to date. 20 As these debates raged, however, scien-
tists and lawyers around the country have worked to obviate
the discussions by demonstrating, in the laboratory and the
courtroom, that the only effective fetal protection policy would
entail shutting down virtually all business. The law should
eliminate the need for such measures or for contrivances that
seek to judicially accomplish what should be done by the
legislature.
Finally, employers, who are the backbone of the economy,
have a right to be able to predict the costs of doing business.
An employer who meets contemporary standards of care in its
occupational safety and health program, pays its workers' com-
pensation premiums, and otherwise follows the law should not
have to worry about "end runs" such as a tort suit for prenatal
injury.
VII. A PROPOSED APPROACH

In order to meet the policy goals stated above, legislation
incorporating the following elements is proposed.
1. Require that all WISHA occupational safety and health
standards expressly address prenatal risk.
Exposure standards should comprise limits that are based
on prenatal hazard data, where available. Permissible expo-
sure levels might need to be lowered in some cases.20 2 Based on
exposure routes and susceptibility, standards may also require
ongoing exposure or biological monitoring.20 3 Specific proce-
dures to accommodate pregnancy may be appropriate for early-
acting teratogens. For example, temporary removal with full
pay and seniority may be indicated for some pregnant employ-
ees to the extent compatible with Title VII strictures.20 4 Prena-
201. See articles cited supra note 4.
202. Although not enough data exists to set many intelligent limits, an exception is
lead, for which consensus standards are already being lowered. See AGGIH
ConsideringAdopting Limit for Blood Levels of Exposed Workers, 23 O.S.H. REP. (BNA)
6 (1993).
203. Monitoring of radiation dosage and blood lead levels is already routine.
204. If needed, state antidiscrimination law should be amended in a manner that
accommodates the least intrusive measures reasonably necessary. Testing for early
pregnancy indicators such as human chorionic gonadotropin might also have a place in
tal hazard training that is specific for the stressor in question

should also be required. All of these requirements could be
grafted easily onto existing WISHA standards.
2. Create a WISHA prenatal hazard warning standard.
Employers should be required to provide specific warnings
to each employee. The contents of a minimal warning should be
promulgated by WISHA and should be aimed at making
employees fully aware of all incurred risks. Accordingly, those
warnings should address workplace prenatal hazards, hazards
of individual lifestyle, and the interrelation of the two. The
warnings should be based on tort law principles of informed
consent rather than scientific dissertations. Those warnings
should be documented, archived, updated, and refreshed
through mandatory posters and other means.
3. Compensate, through the industrial insurance pro-
gram, children suffering from prenatal injuries and birth
defects resulting from the workplace exposures of their parents.
Such compensation should include medical, rehabilitative,
and, after majority or emancipation, disability pensions. The
standards of causation that apply to occupational disease
claims should be used to determine eligibility, although a rebut-
table presumption in favor of causation should be raised in the
case of certain well-documented parental exposures to known
teratogens/fetotoxins such as lead. Transplacental carcinogens
should also be covered. Statutory time limitations should
accommodate latent periods.
4. Compensate, through the industrial insurance pro-
gram, employees for the medical expenses of miscarriages asso-
ciated with workplace hazards.
This compensation should also be administered under
industrial insurance and should include costs of grief and preg-
nancy counseling. The standards of causation should be lenient
and a presumption of causation should be drawn for any sub-
stance that has been linked to miscarriage by statistically sig-
nificant epidemiological studies.20 5
5. Provide employers who pay into the industrial insur-
ance system and who have, at a minimum, complied with the
prenatal hazard warnings promulgated by WISHA, immunity
from tort liability for prenatal injury and miscarriage.
limited circumstances. At a minimum, employees should be afforded the risk-reducing

options on a voluntary basis.
205. Some formula for reconciling conflicting studies may be necessary.
This immunity should include all co-employees and per-

sonal services contractors and should extend in perpetuity.
Exceptions to this immunity should be made for intentional con-
duct, defined as an intention that the parent be exposed above
a WISHA standard.2 °6 Employers who fail to comply with
WISHA prenatal hazard warnings should lose the immunity
but such noncompliance should not affect the immunity of co-
employees unless a showing is made that no solvent business or
successor remains against which a judgment could be
enforced.2 °7
VIII. CONCLUSION
The science respecting prenatal hazards in the workplace is

rapidly advancing, showing heretofore unknown associations.
It is incumbent on the law to keep up. As it stands today, the
law is not able to provide for children injured by their parents'
exposures, and the law is causing unproductive tension between
employers and women employees. It is time for a more rational
approach.
206. The higher, inappropriate standard being the intention that the prenatal
harm occurs. Where no WISHA standard exists, tort standards of recklessness should
govern.
207. Analogous to WASH. REV. CODE § 7.72.040 (1992).

Liability For Prenatal Harm in The Workplace - The Need For Reform

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Liability for Prenatal Harm in the Workplace:

The Need for Reform*

Fifteen percent of all recognized pregnancies result in spon-

* © Steven S. Paskal, 1994

ing from emotional stress, cigarette smoke, and fall hazards to

II. PRENATAL HARM IN THE WORKPLACE

Most people's conception of prenatal injury revolves around

6. See generally STANLEY W. JACOB ET AL., STRucTuRE AND FUNCTION IN MAN

spermatozoa for fertilization.1" The average ejaculation con-

10. Id. at 580.

The female contributes one of a finite number of ova, each

18. OTA, supra note 1, at 48-49.

If the genetic material of the spermatozoon or the ovum has

histologic finding that a large percentage of spontaneous abor-

the day incurred. 39 Dramatic manifestations of this phenome-

39. CAsARErr & DOULL, supra note 29, at 318.

the first such case reported in the United States.5" As more

workplace exposure to toxins is transmitted to the fetus result-

60. OTA, supra note 1, at 56-57.

case where a woman whose blood does not contain a protein

69. BERKOW & FLETCHER, supra note 19, at 1132.

III. COMPENSABLE REPRODUCTIVE OUTCOMES

While the scientific evidence may implicate an agent with

be cognizable under Washington law to sustain a lawsuit here.

ages. 7 Where death occurs later in life, 8 the child's estate or

mon and obvious endpoints of developmental harm.9" In fact,

IV. THEORIES OF LIABiLITY

Assuming the law recognizes the compensability of an

"foreseeability is not an element of a strict liability claim. Confusion caused by

ful effects of a workplace hazard and an employee's susceptibil-

111. Harbeson, 98 Wash. 2d at 476, 656 P.2d at 493.

injury, may also face liability. 11 7 For co-employees, this liability

Conflicting policy considerations make the task of defining

more than evidence of the requisite standard of care, leaving

unmindful of the fact that a claim for prenatal injuries is prone

hint of a possibility that the [spermicide] causes birth

137. Id. at 294.

oxia. In such cases, the question of causation is relatively

Although the types of damages allowable in Washington

occupational impairment is compensated by monthly payments

151. WASH. REV. CODE § 51.32.060 (1992). Different compensation is afforded to

V. DEFENSES TO EMPLOYER LIABILITY

In most workplace injury scenarios, employers may invoke

A. Workers' Compensation Exclusivity

Texas Court of Appeals ruled that the workers' compensation

derivative of injury to the mother and thus barred by the state's

B. Compliance with Title VII

By invoking Johnson Controls, an employer who has com-

C. Compliance With Safety Regulations

behavior may result in different legal outcomes depending on

In Washington, "[a] parent does not have legal authority to

ineffective. Similarly, an agreement to waive a future claim

VI. THE POLICY GoALs OF A SOLUTION

A problem clearly exists. Many prenatal injuries are proba-

The incentive to exclude women should also be eliminated.

VII. A PROPOSED APPROACH

tal hazard training that is specific for the stressor in question

limited circumstances. At a minimum, employees should be afforded the risk-reducing

This immunity should include all co-employees and per-

The science respecting prenatal hazards in the workplace is

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